Nonsteroidal Anti-inflammatory Drug (NSAID) Tolerance After Biological Therapy in Patients With NSAID-Exacerbated Respiratory Disease: A Randomized Comparative Trial

Sánchez, Jorge; García, Elizabeth; López, Juan-Felipe; Calle, A.; Buendia, Jefferson-Antonio

doi:10.1016/j.jaip.2023.04.033

Cited by 8 publications

(2 citation statements)

References 40 publications

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“…As for NERD, dupilumab suppresses urinary LTE4 production and improved asthma symptoms in patients with NERD [81]. Furthermore, recent studies have suggested that dupilumab increases aspirin tolerance in patients with NERD [82,83], suggesting that IL-4/IL-13 contributes to the pathogenesis of NERD.…”

Section: Effects Of Il-4/il-13 Blocking On Severe Asthmamentioning

confidence: 99%

The Possible Roles of IL-4/IL-13 in the Development of Eosinophil-Predominant Severe Asthma

Nakagome,

Nagata

2024

Biomolecules

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Bronchial asthma is characterized by airway inflammation, airway hyperresponsiveness, and reversible airway obstruction. Eosinophils contribute to the pathogenesis of airway disease mainly by releasing eosinophil-specific granules, lipid mediators, superoxide anions, and their DNA. Type-2 cytokines such as interleukin (IL)-4 and IL-13 also play roles in the development of bronchial asthma. Among these cytokines, IL-4 is involved in T-cell differentiation, B-cell activation, B-cell differentiation into plasma cells, and the production of immunoglobulin E. Although IL-13 has similar effects to IL-4, IL-13 mainly affects structural cells, such as epithelial cells, smooth muscle cells, and fibroblasts. IL-13 induces the differentiation of goblet cells that produce mucus and induces the airway remodeling, including smooth muscle hypertrophy. IL-4 and IL-13 do not directly activate the effector functions of eosinophils; however, they can induce eosinophilic airway inflammation by upregulating the expression of vascular cell adhesion molecule-1 (for adhesion) and CC chemokine receptor 3 ligands (for migration). Dupilumab, a human anti-IL-4 receptor α monoclonal antibody that inhibits IL-4 and IL-13 signaling, decreases asthma exacerbations and mucus plugs and increases lung function in moderate to severe asthma. In addition, dupilumab is effective for chronic rhinosinusitis with nasal polyps and for atopic dermatitis, and IL-4/IL-13 blocking is expected to suppress allergen sensitization, including transcutaneous sensitization and atopic march.

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Section: Effects Of Il-4/il-13 Blocking On Severe Asthmamentioning

confidence: 99%

The Possible Roles of IL-4/IL-13 in the Development of Eosinophil-Predominant Severe Asthma

Nakagome,

Nagata

2024

Biomolecules

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“…A real-life retrospective study involving 74 individuals who received biologicals for AERD reported that patients who received dupilumab benefited from a significant reduction in SNOT-22 quality of life scores and reduced use of oral corticosteroids and antibiotics, whereas anti-IgE or anti-IL-5/IL-5Rα showed no statistically significant results. 107 …”

Section: Efficacy In Patients With Crswnp and Aerdmentioning

confidence: 99%

Brazilian guideline for the use of immunobiologicals in chronic rhinosinusitis with nasal polyps ‒ 2024 update

Anselmo-Lima,

Romano,

Tamashiro

et al. 2024

Brazilian Journal of Otorhinolaryngology

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Hat die ASS-Desaktivierung in Zeiten von Biologika noch einen Stellenwert bei chronischer Rhinosinusitis mit nasaler Polyposis?

Klimek,

Förster-Ruhrmann,

Hagemann

et al. 2024

HNO

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Nonsteroidal Anti-inflammatory Drug (NSAID) Tolerance After Biological Therapy in Patients With NSAID-Exacerbated Respiratory Disease: A Randomized Comparative Trial

Cited by 8 publications

References 40 publications

The Possible Roles of IL-4/IL-13 in the Development of Eosinophil-Predominant Severe Asthma

The Possible Roles of IL-4/IL-13 in the Development of Eosinophil-Predominant Severe Asthma

Brazilian guideline for the use of immunobiologicals in chronic rhinosinusitis with nasal polyps ‒ 2024 update

Hat die ASS-Desaktivierung in Zeiten von Biologika noch einen Stellenwert bei chronischer Rhinosinusitis mit nasaler Polyposis?

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